scholarly journals Ribosome biogenesis adaptation in resistance training-induced human skeletal muscle hypertrophy

2015 ◽  
Vol 309 (1) ◽  
pp. E72-E83 ◽  
Author(s):  
Vandre C. Figueiredo ◽  
Marissa K. Caldow ◽  
Vivien Massie ◽  
James F. Markworth ◽  
David Cameron-Smith ◽  
...  

Resistance training (RT) has the capacity to increase skeletal muscle mass, which is due in part to transient increases in the rate of muscle protein synthesis during postexercise recovery. The role of ribosome biogenesis in supporting the increased muscle protein synthetic demands is not known. This study examined the effect of both a single acute bout of resistance exercise (RE) and a chronic RT program on the muscle ribosome biogenesis response. Fourteen healthy young men performed a single bout of RE both before and after 8 wk of chronic RT. Muscle cross-sectional area was increased by 6 ± 4.5% in response to 8 wk of RT. Acute RE-induced activation of the ERK and mTOR pathways were similar before and after RT, as assessed by phosphorylation of ERK, MNK1, p70S6K, and S6 ribosomal protein 1 h postexercise. Phosphorylation of TIF-IA was also similarly elevated following both RE sessions. Cyclin D1 protein levels, which appeared to be regulated at the translational rather than transcriptional level, were acutely increased after RE. UBF was the only protein found to be highly phosphorylated at rest after 8 wk of training. Also, muscle levels of the rRNAs, including the precursor 45S and the mature transcripts (28S, 18S, and 5.8S), were increased in response to RT. We propose that ribosome biogenesis is an important yet overlooked event in RE-induced muscle hypertrophy that warrants further investigation.

2018 ◽  
Author(s):  
Brad Jon Schoenfeld ◽  
Bret Contreras

This letter is a response to the paper by Damas et al (2017) titled, “The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis,” which, in part, endeavored to review the role of exercise-induced muscle damage on muscle hypertrophy. We feel there are a number of issues in interpretation of research and extrapolation that preclude drawing the inference expressed in the paper that muscle damage neither explains nor potentiates increases in muscle hypertrophy. The intent of our letter is not to suggest that a causal role exists between hypertrophy and microinjury. Rather, we hope to provide balance to the evidence presented and offer the opinion that the jury is still very much out as to providing answers on the topic.


1997 ◽  
Vol 82 (3) ◽  
pp. 807-810 ◽  
Author(s):  
Arny A. Ferrando ◽  
Kevin D. Tipton ◽  
Marcas M. Bamman ◽  
Robert R. Wolfe

Ferrando, Arny A., Kevin D. Tipton, Marcas M. Bamman, and Robert R. Wolfe. Resistance exercise maintains skeletal muscle protein synthesis during bed rest. J. Appl. Physiol. 82(3): 807–810, 1997.—Spaceflight results in a loss of lean body mass and muscular strength. A ground-based model for microgravity, bed rest, results in a loss of lean body mass due to a decrease in muscle protein synthesis (MPS). Resistance training is suggested as a proposed countermeasure for spaceflight-induced atrophy because it is known to increase both MPS and skeletal muscle strength. We therefore hypothesized that scheduled resistance training throughout bed rest would ameliorate the decrease in MPS. Two groups of healthy volunteers were studied during 14 days of simulated microgravity. One group adhered to strict bed rest (BR; n = 5), whereas a second group engaged in leg resistance exercise every other day throughout bed rest (BREx; n = 6). MPS was determined directly by the incorporation of infusedl-[ ring-13C6]phenylalanine into vastus lateralis protein. After 14 days of bed rest, MPS in the BREx group did not change and was significantly greater than in the BR group. Thus moderate-resistance exercise can counteract the decrease in MPS during bed rest.


2017 ◽  
Vol 313 (3) ◽  
pp. C257-C261 ◽  
Author(s):  
Joaquín Pérez-Schindler ◽  
Mary C. Esparza ◽  
James McKendry ◽  
Leigh Breen ◽  
Andrew Philp ◽  
...  

Although the signal pathways mediating muscle protein synthesis and degradation are well characterized, the transcriptional processes modulating skeletal muscle mass and adaptive growth are poorly understood. Recently, studies in mouse models of muscle wasting or acutely exercised human muscle have suggested a potential role for the transcription factor signal transducer and activator of transcription 3 (STAT3), in adaptive growth. Hence, in the present study we sought to define the contribution of STAT3 to skeletal muscle adaptive growth. In contrast to previous work, two different resistance exercise protocols did not change STAT3 phosphorylation in human skeletal muscle. To directly address the role of STAT3 in load-induced (i.e., adaptive) growth, we studied the anabolic effects of 14 days of synergist ablation (SA) in skeletal muscle-specific STAT3 knockout (mKO) mice and their floxed, wild-type (WT) littermates. Plantaris muscle weight and fiber area in the nonoperated leg (control; CON) was comparable between genotypes. As expected, SA significantly increased plantaris weight, muscle fiber cross-sectional area, and anabolic signaling in WT mice, although interestingly, this induction was not impaired in STAT3 mKO mice. Collectively, these data demonstrate that STAT3 is not required for overload-mediated hypertrophy in mouse skeletal muscle.


2008 ◽  
Vol 33 (3) ◽  
pp. 470-475 ◽  
Author(s):  
Joel R. Krentz ◽  
Braden Quest ◽  
Jonathan P. Farthing ◽  
Dale W. Quest ◽  
Philip D. Chilibeck

High doses of ibuprofen have been shown to inhibit muscle protein synthesis after a bout of resistance exercise. We determined the effect of a moderate dose of ibuprofen (400 mg·d–1) consumed on a daily basis after resistance training on muscle hypertrophy and strength. Twelve males and 6 females (~24 years of age) trained their right and left biceps on alternate days (6 sets of 4–10 repetitions), 5 d·week–1, for 6 weeks. In a counter-balanced, double-blind design, they were randomized to receive 400 mg·d–1 ibuprofen immediately after training their left or right arm, and a placebo after training the opposite arm the following day. Before- and after-training muscle thickness of both biceps was measured using ultrasound and 1 repetition maximum (1 RM) arm curl strength was determined on both arms. Subjects rated their muscle soreness daily. There were time main effects for muscle thickness and strength (p < 0.01). Ibuprofen consumption had no effect on muscle hypertrophy (muscle thickness of biceps for arm receiving ibuprofen: pre 3.63 ± 0.14, post 3.92 ± 0.15 cm; and placebo: pre 3.62 ± 0.15, post 3.90 ± 0.15 cm) and strength (1 RM of arm receiving ibuprofen: pre 18.6 ± 2.8, post 23.4 ± 3.5 kg; and placebo: pre 18.8 ± 2.8, post 22.8 ± 3.4 kg). Muscle soreness was elevated during the first week of training only, but was not different between the ibuprofen and placebo arm. We conclude that a moderate dose of ibuprofen ingested after repeated resistance training sessions does not impair muscle hypertrophy or strength and does not affect ratings of muscle soreness.


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